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Pulmonary - Flashcards
Flashcard Deck Information
| Class: | PADP 6200 - History and Physical Exam I |
| Subject: | Physician Assistant Studies |
| University: | East Carolina University |
| Term: | Fall 2009 |
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Anatomic segments of the respiratory tract (4)
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Naso-oropharynx (upper airway) Conducting airways (Larynx, trachea) Respiratory bronchioles Alveolar ducts |
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Upper airway functions
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Warms and humidifies air Nasal hairs and turbinates filter out large particles. |
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Conducting airway function
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Decelerates velocity of air molecules Furthers cleanses air of particulates |
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Respiratory bronchiole function
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Last "filter zone" to clear small particles from inspired air. Histological boundary. Cuboidal epithelium ends, Type I Alveoli begin. End of mucous secreting cells. Immune defense changes emphasis to macrophages, inflammatory cells, opsonins. |
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Alveolar ducts and space
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Site of gas exchange across a thin layer of type I alveolar epithelial cells. Alveoli intertwined with a meshwork of pulmonary capillaries. Surface area approx 130 sq ft, "tennis court" |
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Relevant Hx items for lung disease
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Smoking, including secondary exposure Occupational and/or environmental exposures (pollution or industrial) Exposure to animal dander FHx: Asthma, allergies, cystic fibrosis (CF), lung cancer, emphysema, alpha-1 antitrypsin deficiency Medication Hx: ACE, opioids |
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Relevant PE findings for lung disease
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Obesity: predisposition for obstructive sleep apnea (OSA) Obesity affects the mechanics of breathing. Increased AP diameter beyond 2:1 ratio (barrel chest) may indicate COPD Kyphoscoliosis; posture causes breathing restrictions Accessory muscle use: laboring from breath. |
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Wheezing
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High pitched respiratory sounds Not always true but, Inspiratory wheeze: more likely upper airway Expiratory wheeze: more likely lower airway ...because exhalation produces collapse of the non-cartilaginous parts of the bronchial tree. |
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Rales/Crackling
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Increased luminal fluid. Popping as collapsed alveoli open up. Associated with pneumonia, COPD |
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Clubbing of the fingers
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Associated with long term hypoxemia from cystic fibrosis, severe bronchiectasis, or congenital heart disease. Spongy nail bed Nail bed angle greater than 180 degrees. |
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Cough mechanism
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Voluntary action or involuntary reflex mediated by the brain. May have a CNS cause, as in ACE-I side effect. Afferent stimuli from the tracheobronchial tree, especially the carina and larynx. May be chem or mech stimuli. Purpose is to clear the airway in response to aspirated objects, noxious aerosols, to clear mucous, foreign particles, or respiratory pathogens. |
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Complications of excessive/chronic cough
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May impair respiration and disrupt sleep. May interfere with social functioning. Other complications: Bronchospasm closing off airways Syncope due to insufficient breath. Rib fractures due to force of muscle contractions Vomiting, urinary stress incontinence Pain (throat, chest, back) |
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Transient/Acute cough
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Inflammatory reaction of trachea or bronchial branches due to infection. Most commonly due to URI, may persist for 6-8 weeks. Noxious vapors Aspirated objects or liquids Pulmonary emboli Pulmonary edema |
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Chronic cough
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Most commonly is chronic bronchitis due to second hand smoke exposure. Other causes are generally based in chronic inflammation (persistetn infection, allergy) or gross anatomical anomaly (tumor, GERD, enlarged left atrium) |
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Asthma and cough
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May be the first symptom of asthma. Inflammatory reaction. Usually a non-productive cough. Can cause the person to wake at night. |
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Sinusitis and cough
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Persistent nasal secretions (also nasal drainage in rhinorrhea) can trigger the cough reflex to clear fluid. |
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GERD and cough
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Regurgitation of gastric contents. ??? |
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ACE Inhibitors and cough
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The hypertension medication can at upon the CNS to trigger the cough reflex in the CNS. Dry, persistent cough. |
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Tumors and cough
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Tomors in the tracheobronchial tree or mediastinal or espophagus can trigger meachanoreceptors. Also aortic arch aneurysm, enlarged left atrium. |
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Dyspnea
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Difficulty breathing (increased mechanical work or ventilation drive) May be described as "shortness of breath" or "air hunger" May be due to circulatory or respiratory reasons |
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Acute dyspnea causes
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Asthma Pulmonary infection Pulmonary edema Pneumothorax Pulmonary embolus Metabolic acidosis ARDS (Acute Respiratory Distress Syndrome) |
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Causes of mechanical work dyspnea
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Decreased lung compliance Increased airway resistance Thoracomuscular dysfunction |
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Causes of increased ventilatory drive
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Increased sensory stimuli Increased chemical stimuli Primary CNS stimuli (voluntary or involuntary) |
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Orthopnea and Nocturnal dyspnea
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May be due to asthma, GERD, Left ventricle dysfunction, obstructive sleep apnea. Rapid onset orthopnea suggests phrenic nerve impairment |
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Paroxysmal nocturnal dyspnea
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Occurs 30 min to 2 hrs after sleeping. Relieved by sitting/standing Most likely cardiac |
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Chronic dyspnea
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Usually COPD, interstitial lung disease, pulm vascular disease, fixed airflow obstruction, pulm fibrosis. Symptoms first appear with exertion, progresses until dyspnea occurs with minimal activity or at rest. Increasingly recognized as a quality of life issue in dying patients. Conflict in that tx can hasten death. |
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Episodic dyspnea
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Suggests CHF (congestive heart failure), asthma, chronic bronchitis, recurrent PE (pulm emboli) |
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Evaluating dyspnea
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CBC (complete blood count): anemia Renal function test: blood pH chest x-ray: fluid, consolidations, obstructions spirometry: obstructive or restrictive lung disease oximetry: perfusion to tissues No Dx apparent? Arterial blood gas and vent/perfusion scan Over 40 or FHx of heart disease? EKG screenings. |
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V/Q scan
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Ventilation-perfusion scan Compares airflow to gas exchange Used to assess for pelmonary embolism |
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Tx of dyspnea
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O2 increases survivial of the hypoxemic, but can lower the respiratory drive. Pulmonary rehab can increase respiratory function in individuals with chronic dyspnea. Benzodiazepine can be used to reduce the aggravating effects of stress/anxiety on dyspnea. Quit smoking to limit damage. Opioids blnt dyspnea but drop the respiratory drive. Fans help the psychological overlay. |
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Chest pain
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Common symptom of lung disease Easily mistaken for cardiac pain, distinguishable by lack of relation to exertion of radiating pain to arm/jaw. |
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Pain due to pleuritis
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Sharp and severe. worsened by breathing |
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Pericarditis pain
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Pain may not be related to breathing, often relieved by leaning forward. |
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Pain from pulmonary embolism
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Feeling of anterior chest pain that may persist for hours. |
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Hemoptysis
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Expectoration of blood originating BELOW the vocal chords. Bronchial arterial circulation is the most common source. May arise from the airways, the pulmonary vasculature, or the pulmonary parenchyma. Most common cause is pneumonia or pulmonary infection. Pulmonary TB is a prominent causes (assoc with night sweats, fever) |
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Hemoptysis seen with acute bronchitis
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In an otherwise healthy person, doesn't warrant extensive evaluation. |
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Hemoptysis w/o infection
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In absence of infection, can be due to a lung tumor. Requires evaluation by chest x-ray, CT scan, and bronchoscopy. Pulmonary embolus leading to infarction almost always results in hemoptysis. |
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Non-pulmonary or atypical hemoptysis
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A small number of patients may have transient, mild, idiopathic hemoptysis. Blood my also come from the upper airway or reflux from the GI tract and stimulate a cough. |
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Hemoptysis and CF
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Hemoptysis may occur in cystic fibrosis and may be life threatening. |
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Massive hemoptysis
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Defined as any amount that is hemodynamically significant. |
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Tx of Hemoptysis
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Identify and treat the specific cause. If "massive hemoptysis", it is life-threatening and both the airways and the circulatory blood volume must be stabilized. Bronchoscopy can localize bleeding and emboli in 85% of cases Cautery can be used to control blood loss. |
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Resonant percussion
Midline trachea
Vesicular breath sounds
A few transient crackles at lung base
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Normal breath Tracheobronchial tree and alveoli clear, pleurae are thin and close, mobility of chest wall is unimpaired |
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Resonant percussion
productive cough
scattered coarse crackles in early inspiration
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Chronic bronchitis Bronchi are inflamed and productive. May develop an airway obstruction |
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Late inspiratory crackles, possible wheezing
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Early left-sided heart failure Increased pressure in pulmonary veins causing congestion, interstitial edema. Bronchial mucosa may become edematous |
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Dull percussion, late insp crackles, increased fremitus and bronchial sounds over an area. Bronchophony, egophony, whispered pec
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Consolidation Alveoli filled with fluid or RBCs Pneumonia, pulm edema, pulm hemorrhage |
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Specific area as dull percussion, absent lungs sounds and fremitus or voice sounds in affected area
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Atelectasis (Lobar obstruction) A plug in the mainstem bronchus (mucous, aspirated object) obstructing airflow, affected lobar area collapses into an airless state. Trachea may be shifted towards the involved side Lung sounds and fremitus, voice sounds are USUALLY absent. Exception is the right upper lobe, which may transmit tracheal sounds. |
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Right lung is dull to percussion, decreased lung sounds and fremitus/voice, stronger at top of lung. Trachea shifted to the left
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Pleural effusion Fluid accumulating in pleural spaces separates air-filled lung from chest wall, blocking the transmission of sound. If a large effusion, it will shift the trachea away from the effusion. May also have a pleural rub. |
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Hyperresonant left lung, decreased lung sounds and fremitus/voice. Right shifted trachea.
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Pneumothorax Air in the pleural space causes lung to recoil from the chest wall, blocking lung sounds in the affected area. Affected area may be hyper-resonant or tympanitic |
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Diffusely hyperresonant lungs, decreased to absent lung sounds, fremitus, voice.
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COPD Slowly progressive disorder in which distal air spaces enlarge and become hyperinflated. Often assoc with chronic bronchitis, is so, crackles, wheezes, or ronchi may be present. |
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Resonant to diffusely hyperresonant lungs
Wheezing, crackling, decreased fremitus and voice sounds
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Asthma Narrowing of the tracheobronchial tree diminishes airflowing, severity fluctuates. During acute attacks the airflow decreases, hyperinflating the lungs. |
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Vertical line of the chest
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Sternal line Midclavicular line Anterior axillary line-from anterior axillary fold Midaxillary line-from apex of axilla Posterior axillary line- from posterior axillary fold Scapular line Vertebral line |
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Lower border of the lungs at 3 lines
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At midclavicular line: rib 6 Midaxillary; rib 8 Posteriorly: at the level of the T10 spinous process |
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Oblique fissure
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Present in both lungs From T3 spinous process to the rib 6 at the midclavicular line Left lung, divides the Upper and Lower Right lung, divides Middle and Lower |
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Horizontal fissure
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Present in the right lung only Starts at the 4th rib anteriorly, meets the oblique fissure at rib 5 along the midaxillary line |
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Locating the RML
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Anterior only Inferior to 4th rib anteriorly, (2 below Sternal angle) Inferior border, rib 6 at mid clavicular |
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T3 spinous process
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Landmark for the divison of Upper Lobes from Lower Lobes on the posterior suface |
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Bifurcation of the trachea
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Trachea bifurcates into mainstem bronchi at T4/Sternal angle |
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Scalene muscles
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Run from sternum to ribs 1 and 2 |
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Parasternal muscles
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Run from sternum to the ribs |
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Frequent causes of chest pain in kids
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Costochondritis Anxiety |
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Common/Concerning Symptoms (5)
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Chest Pain Shortness of Breath (dyspnea) Wheezing Cough Blood-streaked sputum (hemoptysis) |
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Potential causes of chest pain (8+)
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Myocardium: angina pectoris, MI Pericardium: Pericarditis Aorta: Dissecting aortic aneurysm Trachea/large bronchi: bronchitis Parietal pleura: pericarditis, pneumonia Chest wall: Costochondritis, HZV Esophagus: Reflux, esophageal spasm Extrathoracic structures: cervical arthritis, biliary colic, gastritis |
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Pain in the lungs:
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Lung tissue lacks pain receptors Pain is usually due to musculoskeletal pain, or inflammation of parietal pleura (not visceral pleura) |
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Assessing dyspnea
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Determine severity based on change in ADLs In dyspnea, SOB is usually related to various activities Anxious patients tend to present as feeling "smothered" or unable to breathe even at rest, and may experience paresthesias. Either may present audible wheezing |
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Wheezing
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Audible, musical respiratory sound suggest partial airway obstruction from secretions, tisue inflammations or a foreign body. |
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Cough
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Reflex response due to irritation of receptors in larynx, trachea, or large bronchi. Usually respiratory, but may be cardio in origin (CHF) Stimuli can be: Pus, blood, mucus, dust, foreign bodies, hot/cold air, inflammation of mucosa, pressure on airways due to enlarged lymph nodes or tumors. |
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Duration of cough
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Acute: less than 3 weeks Subacute: 3-8 weeks Chronic: 8+ weeks |
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Causes of acute cough
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Usually viral URI also: Acute bronchitis Pneumonia CHF Asthma Foreign body |
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Cause of subacute cough
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Postinfectious coughing (clearing old mucous) Bacterial sinusitis Asthma |
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Causes of chronic cough
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Post nasal drip Asthma GERD Chronic bronchitis Bronchiectasis |
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Mucoid sputum
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Translucent white or grey |
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Purulent sputum
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Creamy, may be yellowed to greenish depending on age |
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Foul smelling sputum
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signifies anaerobic bacteria, lung abcess |
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Tenacious sputum
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Suggests cystic fibrosis |
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Quantifying sputum production
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Ask patient to estimate volume per 24 hours (tsp, tbsp, cup, liter?!?) |
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Origin of blood in cough
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May be along any point in the respiratory tract, but may also be washing up from the GI tract, then triggering cough a la GERD. GI blood is usually darker, may be mixed with food. |
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Hemoptysis in children
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Rare, usually seen in conjunction with cystic fibrosis |
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Smoking elevates risk for:
(5)
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Coronary artery disease Stroke Peripheral vascular disease COPD mortality Lung cancer mortality |
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Risks to non-smokers
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Elevated risk of Asthma Lung cancer Ear and Respiratory infections Residential fires |
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5 "A"s of smoking
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Ask about tobacco use Advise to quit through clear, personalized messages Assess willingness to quit Assist to quit Arrange follow up and support |
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Influenza vaccne populations
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Adults with chronic pulmonary conditions, chronic medical illnesses, or immunosuppressed Residents of Nursing homes or Chronic Care Facilities Health Care personnel Household contacts/caregivers of those under 5 or over 50 |
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Strep pneumoniae vaccine populations
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Age 65+ Anyone 2-64 with a chronic illness that raises pneumococcal infection risk: sickle cell anemia, cardio or pulm disease, diabetes, cirrhosis, or CSF leaks Those with or getting cochlear implants The immunocompromised, or those undergoing treatments that will cause it Some Native American groups (Alaska) |
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Normal vesicular sounds
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Soft, low pitch, rustling Heard at peripheral lung fields Inhale 2:1 exhale |
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Normal bronchial sounds
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High, loud Expiratory lasts longer than nspiratory More "Vader"-ish Slight pauses Heard at |
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Silent gap
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Suggests bronchial breath sounds |
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Wheezing
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If expiratory (and likely prolonged) suggests COPD disorder such as asthma, or bronchitis |
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egophony
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"eee" becomes "a" Suggest consolidation Should also be accompanied by abnormally increased fremitus and dullness to percussion. |
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Crackles
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May be due to transudate, infection, fluid, or loss of elasticity as in emphysema. Pneumonia, fibrosis, early CHF |
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Clearing of crackles after change in position or cough
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Suggests inspissated secretions, bronchitis or atelectasis |
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Increased transmission of voice sounds
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Suggests that air filled lung has become airless. |
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Upper anterior lung fields
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tend to be louder for normal vesicular sounds |
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Stridor
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high pitched, audible sound, normally inspiratory Upper airway obstruction Assoc with croup or aspirated objects in kids Sounds reedy |
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Bronchophony
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Voice sounds are transmitted better than they should be because of fluid or solid mass where there should be air. |
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Whispered pectoriloquy
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In a normal lung, whispered words are almost inaudible due to air's poor sound condection. In a consolidated lung field it is easier to hear the whispered word. |
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Squeezing the sternum and spine
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Tests for rib fracture by causing agonizing pain. |
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Absent breath sounds
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Mucus plug in bronchi prevent airflow, causes collapse (atelectasis/lobar obstruction Exception to absent sound is the RUL atelectasis, which can pick up trachea sounds Trachea may be shifted TOWARD the collapsed side. |
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Bronchial sounds, late crackles, increased B/E/WP, dull percussion
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Suggest consolidation over the area |
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Pneumothorax VS Atelectasis
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Trachea may shift in either, but in opposite directions. Pneumo: hyperresonant Atelectasis: dull |
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Diffuse resonance to hyperresonant, with wheezing, decreased voice sounds
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Asthma, due to hyperinflation |
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Diffuse hyperresonance, decreased breath sounds, fremitus, voice. Possible crackles or ronchi
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COPD |
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Early inspiratory crackles
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Chronic bronchitis if normal resonance COPD if hyperresonant Also, asthma |
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Late inspiratory crackles
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(Early) CHF edematous, congested pulmonary vein OR interstitial lung disease, such as fibrosis |
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Mediastinal crunch
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Crackles synchronous with heartbeat Best heard in left lateral position Due to mediastinal emphysema AKA Hamman's Sign |
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Pleural rub
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Creaking or rasping sounds Usually painful, patient may be guarding, avoiding deep respirations (rapid shallow instead) |
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Normal adult thorax
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2:1 wider than deep |
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Pectus excavatum
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Depression of the sternum deeper than ribs Compression of the heart and great vessels may cause murmurs |
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Barrel chest
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Increased anteroposterior diameter Babies, the elderly, COPD |
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Pectus carinatum
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Sternum is more anterior than usual, causing the costal cartilage to be depressed |
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Traumatic flail chest
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Multiple rib fracture cause paradoxical movements (damaged area of chest wall collapses on inspiration, expands on expiration) |
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Thoracic kyphoscoliosis
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Kyphosis and scoliosis distort normal alignment of ribs, lungs Complicates lung finding. One side hyperflexed, other is hyperextended. No symmetry. |
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Sticky, red, jelly like sputum
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Klebsiella |
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Acute Respiratory Failure
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Respiratory dysfunction leading to abnormal blood gas values Unlike COPD, acute, not chronic Defined as a significant change from baseline, almost always with significant hypoxemia. Potentially fatal |
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ARF blood values
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Often defined as Pa-O2 of less than 55 mmHg Pa-CO2 50 mmHg or higher if accompanied by arterial acidosis w/ pH of 7.3 or less Normal values: |
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Mechanisms leading to hypoxemia
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Decreased inspired partial pressure of O2 (altitude) Hypoventilation V/Q mismatch Shunting of blood Abnormal O2 diffusion |
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Objectives in diagnosing ARF
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Confirm ARF is present Dx type of ARF (hypoxic, hypercapnic, or both) Determine the specific causes |
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Causes of hypoxic ARF
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Acute lung injury/ARDS Pneumonia Pulm Emboli Acute lobar atelectasis Pulmonary edema Lung contusion Acute Collagen-vascular disease (Systemic Lupus. etc) Generally, disease which impair gas diffusion affect O2 first |
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Causes of hypercapneic-hypoxic ARF
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COPD Kyphoscoliosis Asthma Ankylosing spondylitis Drugs causing resp depression GB syndrome Obesity hypoventilation syndrome Acute MG Spinal cord tumors Metabolic Generally, diseases of poor respiratory movement |
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Asterixis
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Symptom of hypercapnia "liver flap" When hands held in "stop" posture, wrist flaps down |
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Clincal manifestations of hypoxemia
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Tachycardia or Bradycardia Hypertension or Hypotension Anxiety Confusion Altered mental Status Cyanosis Seizures Lactic acidosis (due to reliance on anaerobic metabolism) |
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Clinical manifestations that can be either hypoxia or hypercapnia
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Diaphoresis Coma |
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Clinical manifestations of hypercapnia
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Somnolence Lethargy Restlessness Tremor Slurred Speech Headache Asterixis Papilledema |
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3 likely outcomes of chest x-ray in ARF
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May show: Normal lungs : COPD, asthma Localized alveeolar filling opacities: pneumonia, PE, atelectasis, infarction Diffuse opacities: Pulmonary edema, acute lung injury, diffuse pneumonia |
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Goal of tx in ARF
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Improve hypoxemia Improve acidosis if life threatening Maintain/improve cardiac output Treat underlying disease process Avoid predictable complications |
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ARF in COPD
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Assoc w/ mortality 6 to 20% ARF may present in odd ways, such as changes in mental status, arrythmias Commonly precipitated by infection (comm acquired pneumonia? Usually atypical pathogen like enteric bacteria or Legionella) |
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TX of ARF in COPD
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Decision to use mech ventilation must be made on clinical grounds. COPD patient already has abnormal blood gas values. |
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Complications in ARF
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3 key problems: DVT, PE, gastric stress ulcers Prevention: H2 blockers to reduce ulcer risk Prophylactic heparin use Leg compression devices Early ambulation: best for avoiding DVT formation Head of bed at 45 degrees |
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ARDS
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Acute Resp Distress AKA acute lung injury Abrupt onset diffuse lung injury characterized by severe hypoxemia and diffuse pulmonary infiltrates Dx requires bilaterla infiltrates, edema due to trauma, not heart failure ARDS if PaO2/F-IO2 is 200 or less |
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Incidence of ARDS
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Usually precipitated by severe sepsis Anually, 40-75 cases per 100,000 Mortality rate 30-50% |
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Physiology of ARDS
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Abnormalities are dominated by hypoxemia with shunting, decreased lung compliance due to injury, increased work to breathe. As disease progresses, fibroproliferation develops, lungs remodel and scar, reducing respiratory capability. |
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Diagnosing ARDS
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Made by acute respiratory distress, severe hypoxemia, diffuse, bilateral infiltrates on chest x-ray. |
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DDx for ARDS
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Must distinguish between cardiogenic pulmonary edema (CHF) and ards Heart info the key. Important for clarifying the underlying cause. |
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Treatment in ARDS
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Respiratory support Treat underlying disease (bacteria, etc) If acute lung injury, PEEP (Positive End Expiratory Pressure) is better than endotracheal intubation, keeps alveoli open during expiration. Inhaled nitric oxide to proven to be useful. Theoretically helps gas exchange. |
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Why ARDS is difficult on nursing
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Important to change between supine and prone position to reduce shunting of blood Prone position may cause facial edema, can be difficult on nursing staff to reposition frequently. |
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Acute Bronchitis
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Bronchi infection Often with viral URI, infectios secretion drain down. Infection causes increased mucous, narrowing the airway and causing shortness of breath |
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Dx acute bronchitis
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Cough longer than 3 weeks Fever, genral symptoms (constituional) Productive cough Common primary care issue esp in winter |
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Etiology of Acute Bronchitis
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Viral or bacterial Influenza Rhinovirus Adenovirus Coronavirus Parainfluenza RSV M. pneumoniae or C. pneumoniae |
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S/S of acute bronchitis
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Productive cough, fever, fatigue and malaise |
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DDx with Acute Bronchitis
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Distinguish between bronchitis and Pneumonia (chest x-ray) Asthma/allergic bronchospasm Congestive heart failure No fever, have other signs, patterns |
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Tx of Acute bronchitis
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Usually self-limited Reserve antibiotics for those with health issues such as COPD, scarring, difficulty clearing mucous, at risk for pneumonia Bronchodilators if difficulty breathing Expectorants to help clear mucous |
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Community Acquired pneumonia
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6th leading cause of death, 12 per 1000 cases annually Risk factors include: Age greater than 60 Smoking Debilitation, bed-ridden folks have less lung expansion, collect more fluid Pre-existing chronic respiratory disease |
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Keys of Community Acquired Pneumonia diagnosis (4)
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Fever and cough Tachypnea and shortness of breath Crackes/rales Positive chest x-ray for effusion/consolidation/infiltrates |
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Traits of S. pneumoniae infection
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Single episode of shaking chill, rigors Rusty sputum fever |
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Walking pneumonia
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Present as less ill due to lower or absent fever Viral or mycoplasm pneumonias |
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Etiology of Community acquired pneumonia
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S. pneumoniae Influenza H. influenzae RSV M. pneumoniae Adenovirus C. pneumoniae Parainflueza S. Aureus M. catarhalis May also be fungal K. pneumoniae Legionella Gram neg rods |
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RSV
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Respiratory Syncytial Virus |
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Symptoms of Community Acquired Pneumonia
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Fever, may or may not have rigors, chills, or sweats Cought, dry or productive Dyspnea Chest pain, esp at area of consolidation Hemoptysis Fatigue/malaise Anorexia |
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Signs of Comm Acquired Pneumonia
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Fever OR hypothermia Tachypnea Tachycardia Decreased O2 saturation Altered breath sounds (area of consolidation) Dullness to percussion (area of consolidation) Rales/crackles |
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DDx for Comm Acquired Pneumonia
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URI/bronchitis Reactive airway disease CHF Broncholitis Obliterating Organzing Pneumonia (BOOP) Lung cancer Pulmonary embolus Atelectasis |
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Lab tests related to Comm Acq pneumonia
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Sputum gram stain and culture (deep cough or sputum induction to get good sample) Blood cultures if sepsis concern ABG's (more accurate than pulse ox) CBC-WBC count Blood chemistry HIV test serology for unusual pathogens; Legionella, M. pneumoniae, C. pneumoniae |
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Imaging results in Comm Acq Pneumonia
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Chest X-ray may show Patchy airspace inflitrates Lobar consolidation Intersitial infiltrates Pleural effusions Effusions may be pus, (empyema) |
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Invasive special studies for pneumonia
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Bronchoscopy: allows imaging, sampling Transthoracic needle aspiration: allows sampling, draining Use if unresponsive to treatment, unsure of the cause of infection |
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Antibiotic Therapy for Outpatient pneumonia
|
Macrolides (clarithromycin 500 mg PO BID) If C. pneumoniae, doxycycline 100 mg PO BID Fluoroquinilones (Levofloxacin 500 mg PO QD) Come back in 2-3 days to check progress If vomiting, can't hold down an oral antibiotic Inpatient tx if: vomiting/need IV, if debilitated, if poor O2 sat |
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General inpatient therapy for comm acq pneumonia
|
Fluoroquinolone or Extended spectrum beta-lactam + macrolide (cefotaxime or ceftriaxone) Usually by IV |
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Antibiotics for ICU patients, comm acq pneumonia
|
Macrolide or fluoroquinolone PLUS extenteded spectrumcephalosporin OR beta-lactam/beta;actamase inhibitor If PCN allergy; fluoroquinolone +/- clindamycin |
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Beta-lactamase inhibitors
|
ampicillin-sulbacatam piperacilin-tazobactam |
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Beta-lactams
|
ceftriaxone cefotaxime |
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Preventing comm acq pneumonia
|
Vaccination! Influenza vaccine Polyvalent Pneumococcal Vaccine Protects aginst 23 strains (also a 6 strain available) Recommended for those age 65+, those with chronic illnesses |
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Hospital acquired pneumonia
|
Different etiology than community, 20-50% mortality rate Occurs MORE than 48hrs after hospital admission Two or more of: Fever Cough Leukocytosis Purulent sputum OR New or progressive parenchymal infiltrate on chest X-ray |
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Most common pathogens of Hospital Acquired Pneumonia
|
P. aeruginosa Opportunistic, not common S. aureus Enterobacter Klebsiella E. coli Unlike community, almost exclusively bacterial, atypical respiratory bacteria |
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Lab Testing in Hospital acquired pneumonia
|
Blood cultures (septicemia/bacteremia) ABGs or Pulse Ox Sputum gram stain, culture Thoracentesis if pleural effusion Goal: ID infection, support respiration |
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Tx of Hospital Acquired pneumonia
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Empiric antibiotics as soon as pneumonia suspected ID organism, tailor therapy to match No uniform consensus on best regimen, by definition, a more complicated patient. |
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Pneumocystis jiroveci background
|
Seen mostly in immunocompromised patients (typically AIDS) and premature or debilitated infants in underdeveloped countries. Unknown transmission, assumed to be airborne |
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Essentials of Dx P. jiroveci
|
Fever, dyspnea, non-productive cough Bilateral diffuse interstitial infiltrates, no lobar consolidation Bibasilar crackles Decreased PaO2 Culture shoes P. jiroveci in sputum, lung tissue, or lavage fluid |
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S/S of P. jiroveci
|
Acute onset of fever, tachypnea, dyspnea, non-productive cough Bibasilar crackles Physical findings may not correlate with severity of disease; may be sicker than they look |
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P. jiroveci lab tests
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Chest X-ray: shows diffuse interstitial inflitrates Isolated elevation of serum LDH levels, but not others Sputum testing for Giemsa stain or PCR |
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Treatment of P. jiroveci
|
Long tx, TMP/SMX (sulfa) 14-21 days of antibiotic admin every 6-8 hours TMP: 12-20mg per kg, daily SMX: 100 mg per kg, daily Bactrim, Septra |
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Tx of P. jiroveci in inpatients or if sulfa-allergic
|
IV or IM Pentamidine, 3 mg per day, 14-21 days Atovaquone 750 mg PO TID for 21 days BUT!! Failure in 15-30% of cases |
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Additional support in tx of P. jiroveci
|
Prednisone started in the first 72 hours of mod/severe pneumonia improves survival **IF** treating the underlying infection Oxygen therapy In HIV patients, prophylaxis is appropriate |
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Prognosis for P. jiroveci patients
|
Infantile form has 20-50% mortality due to lack of access to care Mortality rate is 3% in AIDS patients Mortality rate 30-50% in other immunodeficient patients |
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Essential of TB diagnosis
|
Fatigue, weight loss, fever, night sweats, cough, including hemoptysis Pulmonary infiltrates on chest x-ray usually apical Positive PPD test Sputum smear/culture positve for M. tuberculosis |
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TB background
|
20-43% or world population infected 15 million in US infected, esp the malnourished, homeless, low-income, HIV positive Primary TB is usually clinically silent, T-cells, macrophages wall of the infection. Replicating, but asymptomatic. 10% will develop active form Drug resistance increasing, now about 15% of US patients, esp among IV drug users Slow growing, often asymptomatic disease |
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S/S of TB
|
Slowly progressive constitutional symptoms: malaise, anorexia, weight loss, fever, night sweats Cough progressing from dry to productive, eventually hemoptysis Classic sign is Apical rales, but examination may be normal |
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Imaging tests for TB
|
Chest X-ray Small, homogenous infiltrates, usually apical Swelling of hilar and paratracheal lymph nodes Segmental atelectasis Pleural effusion Cavitation: walled of areas of infection |
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Sputum testing TB
|
3 morning sputum smaples for culture or DNA/RNA amplification Can also use bronchoscopy for imaging/sampling |
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PPD testing
|
Tuberculin skin test 0.1 mL of PPD intradermally Read after 48-72 hours, positive if RAISED red lesion is >5mm in immunocompromised, recent contacts of active TB >10mm for immigrants, IV drug users, high risk employees or children under age 4 >15mm for persons with no risk factors Report positives to the Health Department |
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Tx of Active TB in non-HIV patients
|
Directly Observed Therapy advised for all patients with drug-resistant TB... can't afford to breed further resistance Daily isoniazid, rifampin, pyrazinamide, and ethambutol for 2 months, followed by 4 months on isonazid and rifampin Pyrazinamide contraindicated for pregnant women |
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Treating TB in HIV patients
|
Should be treated by and ID specialist Longer duration of therapy Beware of drug interactions between rifampin and HIV drugs Pyridoxine (Vit B6) 25-50 mg PO QD for all HIV+ patients on isoniazid to reduce nervous system side effects Medications (esp isoniazid) strain liver, check liver enzymes monthly to monitor health. |
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Tx of Latent TB
|
Tx reduces risk of developing active TB from 10% to 1% Isoniazid, 300 mg PO QD for 9 months with supplemental pyridoxine. Rifampin 10mg/kg and pyrazinamide 15-20mg/kg PO QD for 2 months Rifampin only for 4 months Monitor liver enzymes |
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Bronchiolitis background
|
Infection of the bronchioles Common disease in up to 7% of infants, usually in first 2 yrs of life, peak incidence at 6 months Most often viral, esp RSV (>50%) Also parainfluenza, adenovirus, M. pneumoniae High risk infant: premature birth during winter Prophylaxis: Synagis (palivizumab) given IM for 5-6 months (winter season) |
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S/S of Bronchiolitis
|
URI symptoms with gradual onset of respiratory distress with dyspneas, paroxysmal wheezing cough. Irritability Tachypnea (if progresses) Intercostal retractions, belly breathing Diffuse, fine rales DDx with acute asthma. Unlike asthma, x-ray shows scattered consolidations |
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Testing for bronchiolitis
|
Monitor O2 saturation (O2 tent) Nasal swab for RSV culture Chest X-ray shwing hyperinflation (depressed diaphragm) and scattered areas of consolidation. |
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Tx and prognosis of Bronchiolitis
|
Generally self-limted Supportive care, bronchodilators to reduce wheezing if needed May have increased incidence of airway hyperreactivity for several yeats. |
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Croup background
|
aka Acute Laryngotracheobronchitis Common, 50k hospitalizations per year Peaks in autumn, early winter Peak age is 3 mos to 5 yrs Etiology: 75% due to Parainfluenza viruses Also adenovirus RSV M. pneumoniae |
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DDx of Croup
|
Epiglottitis Bronchiloitis Pneumonia Asthma Unlike Bronchiolitis, Pneumonia, no lung consolidations Unlike asthma, fever |
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S/S of croup
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URI with gradual onset of a barking cough, worst on 1st or 2nd day Mild to moderate respiratory distress Worse at night Resolves gradually Some develop worsening stridor and cyanosis Lung sounds usually normal may show Steeple sign on chest x-ray due to narrowed airway |
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Lab testing Croup
|
O2 sats may be decreased WBC normal or slightly elevated Normal chest x-ray, neck x-ray may show "steepl sign" in about 50% of cases |
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Tx of Croup
|
10% of children need to be hospitalized due to respiratory distress, 1-5% of these will need to be intubated. Inpatient tx: cool, humidified air via croup tent Supplemental oxygen Racemic epinephrine via nebulizer Single dose dexametasone, IM Outpatient: one dose Im dexamethasone, night walks to soothe Prognosis: recurrences are common |
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Risk factors for PE
|
Immobility (bedrest, obesity, etc) Hypercoaguable states (meds, disease, gene defect) Increased central venous pressure (low cardiac output, Pregnancy) Hyeperviscosity/Polycythemia Oral contraceptives Vessel damage (prior DVT, surgery, trauma) |
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Pulmonary embolism background
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Common, often fatal complication of venous thrombus formation DVT and PE are different manifesations o the same disease 50k deaths per year 3rd leading cause of death among hospitalized patients |
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Essential of PE Dx
|
Predisposition to thrombosis, esp lower extremities Dyspnea, chest pain, hemoptysis, or syncope Tachypnea and a widened difference between alveolar and arterial PaO2 Visible defects on V/Q scan, spriral CT scan, or pulm angiogram |
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Embolus
|
Most common embolusis thrombolus May arse anywhere in venous circulation or heart, often in the deep venous of the calf muscles. Thrombi of the calf rarely embolize to pulm circulation 20% of calf thrombi propagates to politeal and ileofemoral veins, then embolizes to pulm. 50-60% of patients with DVT will develop PE |
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Non-thrombus emboli
|
Fat, Air, Amniotic fluid, Septic (endocarditis) vegetation on heart valve Tumor, Foreign body (ie, talc in IV drug use), parasite eggs (schistosomiasis) |
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Pathophysiology of PE
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Obstruction of vascular bed, vasoconstriction leads to increased pulmonary vascular resistance. Areas with no blood flow= wasted ventilation/dead space Surfactant depletion causes atelectasis, Right to left shunting occurs, decreased cardiac output, all lead to hypoxemia. Reflexive bronchoconstriction of tramatized tissue. All sum to dyspnea |
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Massive PE
|
presents with systemic arterial hypotension Dyspnea Hypotension Syncope Cyanosis |
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Moderate to large PE
|
RV hypokinesis (impeded RV pumping) but normal systemic arterial pressure |
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Small to moderate PE
|
Normal Right heart function and systemic arterial pressure |
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Small, distal emboli
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Pleuritic pain, cough, or hemoptysis often suggests small embolism located distally near the pleura. General rule: bigger, more systemic Smaller, more pleuritic |
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"Classic Signs" of PE
|
Low grade fever Neck vein distension (JVD) Accentuated pulmonic second heart sound |
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S/S of PE
|
Dyspnea most frequent symptom (75-85%) Tachypnea most frequent SIGN Pain on respiration in 65-75% Low grade fever Neck vein distension (JVD) Accentuated pulmonic second heart sound |
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DDx of PE
|
Other "chest pain with shortness of breath" MI, unstable angina Pneumonia, bronchitis, COPD exacerbations Congestive heart failure Asthma Pericarditis Primary pulmonary hypertension Rib fracture, pneumothorax, costochondritis Always suspect PE! |
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Blood gas changes in PE
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V/Q matching: appropriate contact between alveolar gas and pulmonary capillary blood Mismatch occurs as a result of imbalance, either due to loss of respiratory flow or capillary blood flow. PE can result in both reduced blood flow less fresh air delivered to alveoli. |
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CXR and VQ in PE
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Use chest x-rays to exclude other common lung diseases and to interpret a VQ scan. Most frequent CXR findings are atelectasis, infiltrates, and pleural effusions. VQ scan: distribution of radioactive gas in lungs, defect appears as an area of diminished blood flow. Can give low, med, or high probability of PE, but not definitive. |
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Defing a high proability V/Q scan
|
2 or more segmental perfusion defects. Sufficient to make diagnosis in most cases. |
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CT scans for PE
|
Very sensitive, when available Can detect thrombus in proximal pulmonary arteries |
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Doppler U/S in PE
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Can be used to look for clots, gauge the direction and velocity of flow in a vessel. Effective in DVT |
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Plethysmography
|
Electrical impedance test for thrombus (PE and DVT) Obstructed and patent have different electrical impedance. |
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Gold Standard for PE Dx
|
Pulmonary Angiography Definitive Dx: intraluminal filling defect in more than one projection Secondary findings that are sggestive of PE; abrupt arterial cut-off, asymmetry of flow, or slow filling. (slow or no) |
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When to use Angiography
|
Non-Dx V/Q scans, or when CT is unavailable or inconclusive Negative non-invasive leg studies Any patient where Dx is in doubt, but there is a high clinical pretest probability of PE. Also, use where PE must be established, as when anticoagulation is contraindicated or placement of IVC filter is contemplated. |
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Lab test in PE
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ECG abnormal in 70%, showing sinus tachycardia an non-specific ST-T changes ABG tests show acute respiratory alkalosis due to tachypnic hyperventialation Unhelpful fact: D-Dimer elevated n thrombus. D-dimer is elevated in hospitalized patients, cancers, or following surgery. |
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Mechanical devices to prevent PE
|
TED hose: graduated compression stockings Intermittent pneumatic compression machines |
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Preventative therapy in PE
|
At risk populations: general and orthopedic surgery, neurosurgery, trauma patients, medical patients of AMI, ischemic stroke with impaired mobility, cancer patients, CHF or severe pulmonary disease. Standard pharm therapy: Low dose unfractionated heparin, 500 units SubQ every 8-12 hours |
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Primary and Secondary therapies in PE
|
Primary therapy: clot dissolution with thrombolysis or removal of PE by embolectomy. Reserved for patients at high risk of death from right heart failure. Tx has significant side effects. Secondary: heparin or warfarin to prevent recurrent PE. ECG key for risk stratification for patients with RV dysfunction. Can ID appropriate candidates for primary therapy of PE even if they have normal arterial pressure. |
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Tx of PE
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Anticoagulants. Failure to acheive therapeutic levels within 24hrs is assoc with 5x increase in clot propagation. Standard regimen is to lead with heparin, followed by 6 months of oral warfarin (coumadin). Can reduce risk of death by recurrent DVT/PE by 80-90%. Heparin and coumadin initiated simultaneously due to different mechanism, delay in coumadin onset. |
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Initial Heparin Tx
|
Unfractionated Heparin Initial load: 80 units/kg via IV, followed by maintenance infusion at 18/unit/kg/hr Check (aPTT) activated partial thromboplastin time in 6 hrs Monitor platelets for 2 weeks: watching for HITS, Heparin Induced Thrombocytopenia Syndrome (platelet insufficiency) |
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LMWH
|
Low Molecular Weight Heparin Compared to UFH, LMWH is easier to dose, requires no monitoring, has similar bleed rates and is at least as effective. Can be use in lieu of warfarin, which is contraindicated in pregnancy Injected subQ |
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Warfarin/Coumadin
|
Blocks vit K dependent clotting factors (beware collards) Half to 1/3 as likely to clot as normal Used as anticoagulant for venous thrombosis for at least 6 mos, initiated concurrently with heparin. Adequacy of therapy is monitored with prothrombin time and the International Normalized Ratio, INR. Normal is 1.0, target is 2.5 (2.0-3.0) Category X medication, contraindicated for pregnancy |
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Timelines for anticoagulation
|
3-6 mos for an initial episode with a reversible risk factor. 12 months for an initial, idiopathic episode. 6-12 mos to indefinitely in patients with irreversible risk factors (genetic coagulopathy, etc). Major anticoagulation compliction is the elevated hemorrhaging risk from cuts, bruises. |
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Thrombolytic therapy
|
No evidence in improves mortality Uses streptokinase, urokinase, recombinant tissue plasminogen activators to accelerates resolution within the first 24hrs However, after 1 week, and 1 month of Dx, tx shows no difference in outcome compared to patients treated with heparin and coumadin. |
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Risk of thrombolytic therapy
|
Thrombolytics carry a 10x greater risk of intracranial bleed vs. heparin. Absolute contraindication: active internal bleed, stroke in past 2 mos. Other contraindications: uncontrolled HTN, surgery, or trauma in past 6 weeks Thrombolytics are indicated for patients who are hemodynamically unstable while on heparin. |
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IVC filter
|
For patients with major anticoagulant contraindication or high risk for developing proximal DVT or PE Also for patients with recurrent thromboembolism DESPITE adequate anticoagulation, for chronic recurrent embolism with pulm HTN, and concurrent performance of surgical pulm embolectomy or thrombendarterectomy. |
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Adjunctive therapy in PE
|
Pain relief Supplemental Oxygen Dobutamine: beta-adrenergic agonist with poitive inotropic and pulmonary vasodilating effects to treat right heart failure, cardiogenic shock. |
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Pulmonary embolectomy
|
Rare emergency procedure of last resort, very high mortality rate. Done in rare, critically ill patients where thrombolytic therapy is contraindicated or unsuccessful. |
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When to refer a PE patient
|
All patients evaluated for, or Dx with PEneed to be evaluated by an expert: pulmonologist hematologist internist |
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How heparin and coumadin work
|
Heparin: blocks intrinsic clotting factors activation Coumadin: blocks the Vit K dependent factors of the extrinsic pathway (blocks both synth and action) |
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Common causes of acute upper airway obstruction
|
LIfe-threatening, must me alleviated immediately. Prep for intubation before laryngoscopy, if used. Acute Alleric Laryngitis FB aspiration Laryngospasm Laryngeal edema (burn) or angioedema Trauma Infection: epiglottitis, croup |
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FB aspiration background
|
Most commonly seen in kids age 1-4, food, coins, marbles. In adults, typically food, esp meat. 5th most common cause of unintentional injury mortality in the US |
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S/S of pharyngeal/hypopharyngeally located FB
|
Dysphagia Odynophagia Drooling |
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S/S if Laryngeal located FB
|
Pain Dysphonia Inspiratory Stridor Dyspnea |
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S/S of tracheal FB
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Can cause both inspiratory and expiratory stridor |
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Distal FB aspiration
|
Right bronchi more common than left Unilteral wheezing Unilaterally decreased breath sounds |
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Tx of FB aspiration
|
Allow a concious, coughing patient to try and cough it out. Unconcious patient: Heimlich, Cricothyroidotomy, tracheotomy Definitve removal requires general anesthesia and direct laryngoscopy or rigid bronchoscopy. |
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Laryngospasm
|
Closure of the glottis due to constriction of the intrinsic and extrinsic laryngeal muscles. Often persists long after initial stimulus stops. Occurs more frequently in children, esp following a URI Potential causes: Contact with upper airway receptor on tongue, palate, and oropharynx with (chemical irritant, secretions, blood, water, vomitus, allergen) |
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Obstructive Sleep Apnea
|
Upper airway obstruction due to loss of pharyngeal muscle tone. Patients w/ narrowed airways are predisposed. Ingestion of alcohol or sedatives, nasal obstruction of any causes, can worsen or precipitate the condition. Cigarette smoking, hypothyroidism are risk factors. Most patients are obese, middle age men, necs 16+ inches. |
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S/S of Obstructive Sleep Apnea
|
Daytime somnolence or fatigue, morning sluggishness or cognitive impairment. Recent weight gains, headache, impotence. Loud cyclical snoring with witnessed apneas, resless thrashing in sleep. Systemic hypertension, pulm hypertension with cor pulmonale. Oropharyngeal narrowing due to excess soft tissue. Short, thick neck. Bradydysrythmia followed by tachdysrythmia |
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DDx with Obstructive Sleep Apnea
|
Central Sleep Apnea, Mixed Sleep Apnea Obesity-hypoventilation syndrome/Pickwickian syndrome Narcolepsy Alcohol or sedative abuse Depression Hypothyroidism Seizure disorder |
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Dx of Obstructive Sleep Apnea
|
Overnight Polysomnography is essential. Apneic episode = breath cessation for 10+ sec Hypopnea defined as decrement in airflow, drop in oxyhemoglobin saturation by 4%+ Home screening with home nocturnal pulse ox has high neg predictive value if no desats are seen. |
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Surgical Tx of Obstructive Sleep Apnea
|
Uvulopalatopharyngoplasty: resection of pharyngeal tissue, portion of soft palate and uvula to expand airway. Helpful in about 50% of selected patients. Nasoseptalplasty is gross nasal septal deformity present Tracheostomy definitive, but reserved from life-threatening, refractory cases/ |
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Medications for Tx of Obstructive Sleep Apnea
|
antinarcoleptics |
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Therapies for
Obstructive Sleep Apnea
|
Step 1: weight loss, avoidance of alcohol and hypnotics 10-20% weight loss may be curative CPAP curative in many patients Polysomnography necessary to determine pressure of CPAP required. Prosthetics inserted into the mouth to prevent pharyngeal occlusion is modestly effective, but compliance is limited. |
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Complications and prognosis of
Obstructive Sleep Apnea
|
Complications: Cor pulmonale Life-threatening cardiac dysrythmias Systemic hypertension Prognosis: 75% of patients continue to use CPAP after 1 year. |
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Intersitital Lung Disease
|
Diffuse parenchymal lung disease Heterogenous group (180+) of disorders. Common response to injury: alveolitis and fibrosis of the interalveolar septum. Not truly interstitial. Begins with injury to capillary and epithelial cells, leading to reorganizing of lung parenchyma w/ irreversible fibrosis. Scaring impedes gas exchange. Causes may be: Infections, environmental, drug-related, Primary Pulmonary disorders, Systemic disorders |
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Clinical Manifestations of Interstitial Lung Disease
|
Diminished lung compliance presenting as restrictive lung disease. Insidious onset of dyspnea on exertion and cough. Minimal sputum, fine late inspiratory crackles. Clubbin in 25-40% of patients. Bilateral basilar Velcro-like rale sin most patients. Loss of lung volume with normal or increased flow rates. Decreased diffusiong of CO2, hypoxemia on exertion. CXR: honecombing or ground glass infiltrates. |
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Dx Tests for ILD
|
Chest X-ray High Resolution CT shows greater detail. Bronchoalveolar lavage may provide a specific diagnosis in infection. Transbronchial biopsy in sarcoidosis or miliary TB (diffuse TB) Surgical lung biopsy (open or tansthoracic): gold standard to diagnose Idiopathic Pulm Fibrosis |
|
Idiopathic Fibrosing Interstitial Pneumonia
|
formerly Idiopathic Pulmonary Fibrosis *Most common of the ILDs Typically age 55 to 60 at Dx Slightly more common in males ANA and Rheumatoid Factor are positive in 25% with no documented collagen-vascular disease. |
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Tx and prognosis of
Idiopathic Fibrosing Interstitial Pneumonia
|
Gold standard of Dx: lung biopsy Tx: supportive care Median survival: 3 yrs from Dx Oral steroids may help, 1mg/kg/day, not routinely recommended. interferon not shown to help Intense research currently in anti-fibrotics Lung-transplant for end-stage ILD |
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Sarcoidosis
|
Systemic disease of unknown cause 90% have granulomatous inflammation of the lung. More common in women, peak incidence 20-30s Highest incidence among African Americans, northern Euro whites. |
|
Presentation of sarcoidosis on exam
|
May present with malaise, fever, and dyspnea with insidious onset. Crackles are uncommon Other manifestations: erythema nodosum, uveitis, parotid gland enlargement, lympadenopathy, hepatosplenomegaly. |
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Circumstantial evidence of sarcoidosis
|
Lab finding that may be seen Leukopenia Elevated Sed rate (inflammation sign) Hypercalcemia/hypercalciuria Elevated ACE levels in 40-80% (not specific or sensitive) |
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Radiographic presentation of
Sarcoidosis
|
Bilateral hilar adenopathy Diffuse reticular infiltrates Pleural effusion in less than 10% Poor prognosis if involvement of lung parenchyma |
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Dx of Sarcoidosis
|
Dx usually requires histologic demonstration of noncaseating granulomas in biopsies from patients with typical symptoms/findings. Biopsy not necessary in patient with Stage I findings on x-ray, and strong clinical correlations. |
|
Tx of sarcoidosis
|
Oral corticosteroids for the pulmonary lesions, constitutional symptoms, hypercalcemia. Tx may last months to years. Serum ACE levels usually fall with clinical improvement. 20% with lung involvement have irreversible impairment 5% die from pulmonary insufficiency. |
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Rheumatic ILD
|
Well established association between systemic rheumatic disease and ILD 1600 deaths/yr Rheumatic ILD more common in men Late onset RA Common age at Dx, 50-60 May be induced by gold salts, methotrexate |
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Presentation of Rheumatic Arthritis ILD
|
Tachypnea and bibasilar rales Clubbing in 75% of cases Pleural rub in 20% Lung biopsy shows prominent lymphocytic infiltrate Rheumatoid modules may be present Tx: oral corticosteroids, with or w/o immunosuppressants |
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Systemic lupus erythematosus
|
A rheumatic disease Acute lupus pneumonitits Tachypnea, tachycardia, dyspnea, cough, cyanosis Fever is common Fatal in 2.5% of cases Tx: high dose oral steroids, in refractory cases include azathioprine |
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Systemic Sclerosis
|
ILD is the most common mainfestation of scleroderma Dyspnea, cough, pulmonary hypertension Pulmonary changes may occur as much as 14 years before cutaneous signs No consistently effective tx |
|
Hypersensitivity Pneumonitis
|
Aka: extrinsic allergic alveolitis Non-asthmatic allergic pulmonary disease Mainly an occupational disease, can become chronic Acute illness: malaise, fever, chills, cough, dyspnea, nausea 4-8 hrs after exposure. Interstitial infiltrates of lymphocytes, plasma cells, noncaseating granulomas Tx: Identify and avoid agent. Short term: Oral corticosteroids 0.5 mg/kg/day, 4-6 weeks |
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Pleura composition
|
Pleura is composed of mesothelial cells, secretes glycoproteins rich in hyaluronic acid, descreses friction. Parietal pleura is innervated, nourished by systemic blood. Visceral pleura lacks sensory nerves, blood from pulm circ. |
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Composition of pleural fluid
|
Low protein, similar glucose and pH to blood. Produced by prietal pleura, drained by lymphatics. Usually 5-15 mL in the pleural space. |
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Exudates
|
Formed by increased outpouring from capillaries and cells, or due to blocking of lymphatics |
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Transudates
|
Form from increased hydrostatic pressure or decreased oncotic pressure. |
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Increased pleural fluid
|
Increased pressure in microvascular circulation (CHF) Decreased oncotic pressure (low albumin) Decreased pressure in the pleural space (collapsed lung) Increased permeability (pneumonia) Impaired lymphatic drainage (malignant effusion) Movement of fluid from peritoneal spaces (ascites) |
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S/S of pleural effusion
|
Often presents with pain, dyspnea, cough. Pain usually unilateral and sharp, worse with cough or inspiration, may radiate to shoulder, neck or abdo. Decreased breath sounds Dull percussion, no tactile fremitus Egophony at upper fluid border, where parenchyma is compressed. |
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Radiology of Pleural Effusion
|
CXR shoes blunting and medial displacement of costophrenic angle Elevation of the diaphragm Lateral decubitus film is most helpful (laying on painful side), supine film least helpful. Ultrasound or CT may provide better definition. |
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Thoracentesis in pleural effusion
|
Can be done for dx or tx Diagnostic in about 75% of patients All newly discovered effusions should be tapped. only 30-50 mL required, but up to 1,000-1500 mL can be removed at one time. Contraindications: Bleeding, diathesis, anticoagulation, small volume, or mech ventilation. |
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Diseases thoracentesis can ID
|
Malignancy (biopsy) Empyema- pus TB via gram stain Fungal infection via KOH Chylothorax: high triglycerides Urinithorax: elevated creatine level, suggests kidney failure Esophageal rupture: increased amylase, pH 6.0 |
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Complications of thoracentesis
|
Pain Bleeding Pneumothorax Infection Puncture of liver, spleen About 50% of therapeutic patients have a temporay drop in PaO2 |
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Transudative Effusion
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Heart failure is the most common Typically bilateral, larger on the right. Assoc with cardiomegaly and vascular congestion. Also, liver failure, ascitic fluid moving across diaphragm (usually on the right) Also, nephrotic syndrome due to low albumin |
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Parapneumonic effusion
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Parapneumonic effusion most common cause of exudative pleural effusion, if uncomplicated can be resolved with antibiotics. If purulent, has becteria, then MUST drain. (chest tube) May be due to upper abdo abcess, Fever and dyspnea Elevated hemidiaphragm on x-ray. |
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Upper abdominal abcess
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May cause exudative pleural effusion Fever and dyspnea Elevated hemidiaphragm on x-ray. |
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Esophageal rupture
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Exudative effusion Half of cases due to endoscopy or esophageal dilation Chest pain, dyspnea and dyspahgia, fever About 50% have subcutaneous emphysema |
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TB and exudative effusion
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Fever, cough, chest pain + PPD |
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Hemothorax
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exudative effusion Results from trauma, malignancy, or pulm infract Larger effusions require chest tube drainage. |
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Chylothorax
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Lymph exudative effusion Usually mediastinal malignancy Milk appearance Tx includes drainage of pleural space |
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Malignant effusion
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Most common cause of exudate Most frequently invasion of pleura by lung cancer Cough, pain, dyspnea Abundant RBCs and lymphocytes Pleural fluid cytology positive in 60% Poor prognosis (except breast cancer, small cell lung cancer) |
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Malignant mesothelioma
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Usually asbestos exposure Dyspnea, cough, pain, weight loss Effusion may be massive, bloody Median survival from Dx is 8-12 mos Treated by surgical removal of tumor, chemo. |
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Lung cancer background
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Leading cause of cancer deaths (29% of all) Declining in men, stable in women 5 yr survival rate at 15% (double 30 yrs ago) |
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Dx of Lung Cancer
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New cough or change in chronic cough Dyspnea, hemoptysis, anorexia, weight loss Enlarging nodule of mass, or a persistent opacity/atelectasis, or pleural effusion on CXR or CT Cytology or histology of sputum, pleural fluid, or biopsy |
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Lung cancer risk factors
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Cigarette smoking (in more than 90%) Other exposures: second hand smokes, radon, asbestos, metals, industrial carcinogens. FHx Diseases assoc w/lung cancer Pulmonary fibrosis COPD Sarcoidosis |
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The 5 main histologic categories of lung cancer
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Squamous cell carcinoma Adenocarcinoma (most common) Large cell carcinoma Small Cell carcinoma (worst prognosis... metastasizer) Bronchioloalveolar cell carinoma (rarest) |
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Squamous cell carcinoma
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Bronchial epithelium Typically a central, intraluminal sessile or polypoid mass. More likely to present with hemoptysis More frequently Dx by sputum cytology Spread locally, may be assoc with hilar adenopathy. |
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Adenocarcinoma
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Arise in mucus glands Usually presents as peripheral nodules or mass |
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Large cell carcinoma
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Heterogenous group of relatively undifferentiated tumors Typically have rapid doubling times, aggressive clinical course Present as central or peripheral mass |
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Small cell carcinoma
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Bronchial Begins centrally, inflitrates submucosa to cause narrowing and obstruction. Hilar and mediastinal abnormalities ar common on CXR Most likely has metastasized by the time Dx is made. |
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Bronchioloalveolar carcinoma
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Arises from epithelial cells, in or distal to the terminal bronchioles. |
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SMLC
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Small Cell Lung Cancer Prone to early spread via blood Rarely amenable to resection because not localized Very aggressive course. Median untreated survival is 6-18 weeks. |
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NSCLC
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Non-small cell lung cancer Spreads more slowly May be cured in early stages following resection Responds well to chemo |
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Lung cancer: presentation at Dx
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Anorexia or weight loss in 55-90% New cough or change in chronic cough 60% Hemoptysis in 6-31% Pain in 25-40% |
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Consequences of local lung cancer spread
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Enobronchial obstruction, atelectasis, postobstructive pneumonia Pleural effusion Change in voice due to compromised laryngeal nerve SVC syndrome (compression leading to JVD, edema) Horner's Syndrome |
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S/S of distant lung cancer metastases
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Liver: asthenia and weight loss Brain: headache, nausea, omiting, seizures, or altered mental status. Bone: bone pain |
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Paraneoplastic syndromes
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May precede, flollow, or accompany lung cancer Dx Eaton-Lambert syndrome SIADH (can't concentrate urine) Hypercalcemia Clubbing Increased ACTH Anemia Hypercoagulability Peripheral neuropathy |
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Cisplatin
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Antineoplatic drug, effective in increasing the survival rates in SCLC and NSCLC as a chemo adjunct. |
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TNM system for staging NSCLC
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T: describes size and location of the primary tumor N: number and location of nodal metastastes M: presence or absence of distant metastases Grouped into 4 prognostic categories NOT used in SCLC |
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TNM stage I-II
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Many patients cured thru surgery Tumor, nodes, but no distant metastases |
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TNM stages IIIb-IV
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Patients in these stages do NOT benefit from surgery |
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TNMA stage IIIa
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Locally invasive, may benefit from surgery in certain cases. |
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Staging SCLC
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Micrometastases assumed to be present Limited disease: (30%) tumor is limited to the unilateral hemithorax Extensive: (70%) tumor extends beyond hemithorax Patients w/ limited SCLC benefit from chemo, prophylactic cranial radiation therapy. |
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Limits on resection of NSCLC
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Complete resection not possible if tumor involves the heart, pericardium, great vessels, esophagus, recurrent laryngeal or phrenic nerves, trachea, main carina, or contralateral mediastinal lymph nodes. May not be curative, but may improve quality of life. |
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Adjuvant chemo
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Surgery or radiation followed by antineoplastic chemo drugs. Cisplatin helps stage II disease Not curative for Stage IIIB and IV, but extends overall survival 5-11 months, Palliative chemo improves quality of life, helps with symptom control. |
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Palliative lung cancer therapy
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Debulking via radiation Pain control Symptom control Referral to hospice. |
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COPD
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irreversible chang ein the lungs/airways 3 proceses: Chronic bronchitis Small airways obstruction Emphysema (alveoli destruction) With asthma, 4th most common causes of death in US Usually develops after smoking for at least 20 pack years. |
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Chronic bronchitis
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Presence of chronic cough and sputum production for at least 3 mos/yr for at least 2 consecutive years. Caused by hypertrophy and hyperplasia of mucous secreting glands. Assoc with increased tendency to develop repeat episodes of acute bronchitis. |
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Peripheral airway disease
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Increased resistance in airflow in bronchioles due to narrowed lumen, in smokers Increased bronchiolar smooth muscle Inflammation Irreversible fibrosis Unknown mechanism |
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Two forms of emphysema
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Centrilobular: smokers, upper lobes, involves the promary bronchioles. May have normal distant alveoli Panacinar: involves entire distal ung unit. Can occur through, but manly in lower lobes. Hereditary factor: alpha-1 antitrypsin deficiency. Assoc with early onset panacinar emphysema even in non smokers. |
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COPD S/S
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Usually presents at age 40-50 Cough, sputum, dyspnea Frequent exacerabations. Redeced FEV, progressive dyspnea, lungs remodel to hyperinflate, wheezing No dyspnea until loss of 50% FEV |
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COPD exacerbation
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Increased dyspnea, coug, wheezing, sputum production. Change in sputum color URI in winter is the most common cause of hospitalization for COPD patients. |
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Blue Bloater
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Cyanotic, mild dyspnea, sputum rich cough, normal recoil. COPD is primarily bronchitis. Prominent heart, large vessels |
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Pink puffers
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Severe dyspnea, poor lung recoil, scant sputum, hyperinflatedchest due to flattened diaphragm, relatively small heart. |
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Testing for COPD
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Best in FEV less than 0.70 Fev1/FVC is hallmark CXR not sensitive Chest CT usueful for emphysema |
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COPD DDx
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Asthma Cystic fibrosis Bronchiectasis Eosinophilic granulomas Bronchiolitis Obliterans |
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Tx of COPD
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Stop smoking Bronchodilators for symptomatic releif |
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Theophylline
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Can be used as oral tx for COPD Narrow therapeutic window |
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